This document discusses HIV and its oral manifestations, with a focus on periodontal diseases. It covers the epidemiology and pathogenesis of HIV, describing how it depletes CD4 cells and impacts the immune system. Various oral conditions associated with HIV are described, including oral candidiasis, oral hairy leukoplakia, Kaposi's sarcoma, and necrotizing periodontal diseases. The pathogenesis of HIV-associated periodontal diseases is explained. Treatment protocols for different oral conditions in HIV patients emphasize the importance of infection control and the patient's overall health status.

1. HIV and Periodontium

2. Contents
Introduction
Epidemiology
Pathogenesis
Classification
HIV testing
Oral manifestations of HIV infection
Pathogenesis of HIV associated periodontal diseases
Gingival and periodontal diseases
Periodontal treatment protocol
Conclusion
References

3. Introduction
AIDS
Montagnier et al 1984: lymphadenopathy-associated
virus (LAV)
Gallo et al. 1984: human T-cell leukemia/lymphoma virus
(HTLV-III)
Dr. Suniti Solmon

4. Introduction

5. Epidemiology
UNAIDS, 2004
5th leading cause of death
75% reside in Sub-Saharan Africa, and South east Asia
(Piot et al 2001)

6. Epidemiology
World's third-largest population suffering from HIV
In 2007, AIDS prevalence rate 0.30%—89th highest in
the world.
2.2
2.25
2.3
2.35
2.4
2008 2009
Population (in million) living
with HIV
Population
(in million)
living with
HIV

7. Pathogenesis
Helper T cells, monocytes, macrophages, Langerhans
cells, and some neuronal and glial brain cells

8. R5 virus – macrophages
- predominate during the early stages
X4 virus - later stage of infection
- associated with increased cytopathogenicity
and more rapid T-cell depletion (Connor et al
1993)
Pathogenesis of HIV

9. Pathogenesis of HIV
109 CD4 cells destroyed daily and replacement of only
6–7% of the total CD4 cells each day (Ho et al 1995).Release of virus and
infected T
cells into the blood
CD4 depletion: Cytotoxic
T-cell immune cytolysis.
Continuous replication of
virus occurs in the lymph
nodes

10. Weeks to months after initial exposure acute
symptoms
Acute phase (up to 2 weeks)
Antigenic viremia - extended period of time before
seroconversion occurs
HIV AIDS (12 years or more)
Pathogenesis of HIV

11. B cell not infected
↑ risk for malignancy and infections with microorganisms
such as viruses, mycobacterioses, and mycoses.
↑ risk for adverse drug reactions
Traumatic injury Oral transmucosal viral
transmission allowing infection of circulating host
defense cells.
Pathogenesis of HIV

12. Classification and staging
Centers for Disease Control,1982
Severe immunodeficiency (CD4 count of < 200/mm3 or a
T4 lymphocyte of < 14% of total lymphocytes)

13. Classification and staging
CDC Surveillance Case Classification
Category A: Acute symptoms or
asymptomatic diseases, along with
individuals with PGL, with or
without malaise, fatigue, or low-
grade fever.
Category B: Symptomatic
conditions such as candidiasis;
herpes zoster; OHL ; idiopathic
thrombocytopenia; or constitutional
symptoms of fever, diarrhea, and
weight loss.
Category C: With outright AIDS as
manifested by life-threatening
conditions identified by CD4+ T
lymphocyte levels of less than 200
per cubic millimeter

14. Tests for HIV
• Total lymphocyte count
< 2,000/cumm
• CD4 < 200/cumm
• Thrombocytopenia
• Raised IgG and IgA
Immunological
tests
• Antigen detection : p24
antigen
• Virus isolation
• Antibody detection
Specific tests

15. Oral manifestations
Mealey et al 1996
• Oral candidiasis
• Oral hairy leukoplakia
• Atypical periodontal diseases
• Oral Kaposi's sarcoma
• Oral non-Hodgkin's lymphoma
• Melanotic hyperpigmentation
• Mycobacterial infections
• Necrotizing ulcerative stomatitis
• Miscellaneous oral ulcerations
• Viral infections
• Viral infections (e.g., cytomegalovirus,
molluscum contagiosum)
• Recurrent aphthous stomatitis
• Bacillary angiomatosis

16. Oral manifestations
Oral candidiasis
Most common oral lesion in HIV diseases (90% of
patients)
Diminished host resistance
85% to 95% are associated with Candida albicans
Oral candidiasis ↑ - CD4+ lymphocytes ↓ 200 cells/mm3
(Katz et al 1992)
Lamster et al (1994): 16% - homosexuals
46% - injected drug users

17. Oral manifestations
Pseudomembranous
candidasis (thrush)
Erythematous candidasis
Angular chelitisHyperplastic candidiasis

18. Diagnosis
Oral candidiasis + esophageal candidiasis, a diagnostic
sign of AIDS (Tavitian et al 1986)
Oral manifestations

19. Treatment
Often refractory or recurrent
10% of candidial organisms - resistant to long-term
fluconazole therapy and cross-resistance to itraconazole,
amphotericin B oral suspension and IV amphotericin B
More common when low CD4 counts
HAART - significant decrease in incidence of
oropharyngeal candidiasis and has reduced the rate of
fluconazole resistance.
Oral manifestations

20. Topical antifungal agents
Systemic antifungal agents - ketoconazole, fluconazole,
itraconazole, and amphotericin B
Oral manifestations

21. Oral hairy leukoplakia
Described in the early 1980s and primarily occurs in
persons with HIV infection
Other areas: Dorsum of the tongue, buccal mucosa, floor
of the mouth, retromolar area, and soft palate
Oral manifestations

22. Human papilloma virus, but subsequent evidence
suggests Epstein Barr virus
Candida organisms - secondary invaders and not the
cause
The microscopic confirmation - strong indicator that the
patient will develop AIDS
83% of HIV-infected patients with OHL develop AIDS
within 31 months, 100% of patients with OHL eventually
developed AIDS. (Greenspan et al 1989)
Oral manifestations

23. Differential diagnosis
• Carcinoma
• Frictional and idiopathic keratosis
• Lichen planus
• Tobacco-related leukoplakia
• Psoriasiform lesions
• Hyperplastic candidiasis
Oral manifestations

24. Treatment
• Anti-viral drugs like acyclovir, valcyclovir
• Laser or conventional surgery
• Lesions tend to re-appear once the therapy is
discontinued (Maeley et al 2004)
Oral manifestations

25. Kaposis sarcoma
Rare, multifocal, vascular malignant neoplasm
Described in 1872 - skin of the lower extremities
of older men of Mediterranean origin
Most common in homosexual
or bisexual men
Male-to-female ratio is 20:1
Oral manifestations

26. HIV-infected individuals are 7000-fold more likely to
develop KS (Fleming et al 1998)
Epidemiologic forms
• Classic
• African
• Organ transplant-associated
• AIDS-associated
Classic form - localized and slowly growing lesion
AIDS-associated- much more aggressive lesion
- 71% show oral lesions
Oral manifestations

27. HHV-8
Found in the saliva of patients with high CD4 cell counts
Oral cavity - first or only site of the lesions (60%)
Oral manifestations

28. Gingival involvement may result in alveolar bone
destruction and loss of teeth (Reichert et al 2003)
Differential diagnosis
• Hemangioma
• Hematoma
• Pyogenic granuloma
• Atypical hyperpigmentation
• Sarcoidosis
• Bacillary angiomatosis
• Angiosarcoma
• Pigmented nevi
Oral manifestations

29. Treatment
• No curative treatment
• Laser excision, cryotherapy, radiation therapy,
intralesional injection with vinblastin, interferon-alpha,
sclerosing agents(3% sodium tetradecyl sulfate) or
chemotherapeutic agents
• Nichols et al described the intralesional injection of
vinblastin at a dose of 0.1mg/cm2 using a 0.2 mg/ml
solution in saline
• Median survival time after onset of KS ranged from 7 to
31 months (Chun et al 1995)
Oral manifestations

30. Bacillary angiomatosis
An infectious vascular proliferative disease
Rickettsia-like organisms, Bartonellaceae, Rochalimaea
quintana or others
Gingival BA - red, purple, or blue edematous soft tissue
lesions destruction of periodontal ligament and
bone
More prevalent with low CD4 levels
Treatment - doxycycline or erythromycin +conservative
periodontal therapy and possibly excision
Oral manifestations

31. Oral pigmentation
↑ incidence of oral hyperpigmentation in HIV-infected
individuals (Kumar et al 2003)
Etiology
• Related to prolonged use of drugs such as zidovudine,
ketoconazole or clofazimine
• Zidovudine - excessive pigmentation
of skin and nails
• Pneumocystis carinii infection or
cytomegalovirus or other viral infections
Oral manifestations

32. Atypical ulcers
Higher incidence of recurrent herpetic lesions and
aphthous stomatitis
Herpes simplex virus, varicella-zoster virus, Epstein-Barr
virus, cytomegalovirus
Herpes may involve all mucosal surfaces and extend to
the skin and may persist for months
Neutropenic patients
Oral manifestations

33. Acyclovir (200-800 mg administered five times daily for
at least 10 days) followed by maintenance therapy (200
mg 2-5 times a day)
Recurrent aphthous stomatitis - topical or intralesional
corticosteroids, antimicrobial mouth rinses, oral
tetracycline rinses
Oral manifestations
Recurrent apthous stomatitis Recurrent herpetic lesions

35. Pathogenesis of HIV associated
periodontal diseases
Role of microbes
Harbour both unusual oral organisms(virus and fungi)
and typical periodontopathogens
Murray et al. (1988) - Candida albicans
Candida invasion associated with severity of periodontal
diseases in HIV patients. (Odden et al 1995)
Suppression of the protective arm and stimulation of the
destructive arm of host response

36. HIV virus - suppresses T-helper cells and/or by acting as
a “superantigen” which may provoke an unregulated and
destructive host response (Shirai et al 1992)
Other viruses
Contreras et al 2001
Overgrowth of periodontal pathogens and opportunistic
infections; ↑ secretion of inflammatory mediators
(Slots et al 2000)
↑ incidence of necrotizing forms of periodontal diseases.
Pathogenesis of HIV associated periodontal diseases

37. Murray et al 1989
Pathogenesis of HIV associated periodontal diseases
0
10
20
30
40
50
60
70
80
90
HIV associated
gingivitis
HIV associated
periodontitis

38. Role of host
Greenspan et al 1990
• HIV associated gingivitis : 0.9 to 1.7
• HIV associated periodontits: 0.1 to 0.9
Immune function regulation
Effect on neutrophils
Lynch et al 1991 – IL-1β
Pathogenesis of HIV associated periodontal diseases
• Polyclonal activation of B cells
• Hyperresponsive phagocytosis
• Defective chemotaxis of
monocytes and neutrophils
• Lymphokine production
• Natural killer cell activity
• Response to soluble antigen
• Immunoglobulin production

39. Gingival and periodontal diseases
Linear gingival erythema
Classified as a gingival disease of fungal origin
Precursor to the necrotizing ulcerative periodontal
diseases
Patton et al 2003
LGE - positive predictive value of 70%
NUP - positive predictive value of 50%

40. Histologic evaluation revealed ↑ polymorphonuclear
leukocytes and IgG-producing plasma cells
Treatment
• Follow meticulous oral hygiene procedures.
• If the lesions do not subside after 2-3 weeks, then
systemic antifungal medication (Flucanazole for 7-10
days)
• 2-3 month recall maintenance
Gingival and periodontal diseases

41. Necrotizing ulcerative gingivitis
Ulceration of the interdental papilla with gingival bleeding
and severe pain
Punched out appearance of the interproximal papilla
Affected area typically covered
with a fibrinous pseudomembrane
Gingival and periodontal diseases

42. Treatment
• Cleaning and debridement of affected sites with peroxide
and topical anesthetic
• Avoid tobacco, alcohol and condiments
• Systemic antibiotics such as metronidazole or amoxicillin
Gingival and periodontal diseases

43. Necrotizing ulcerative periodontitis
An extension of NUG in which bone loss and periodontal
attachment loss occurs
Candidial organisms and human herpes virus (Slots et al
2004)
Spirochetes, zones of aggregated polymorphonuclear
leukocytes, and necrotic cells found in NUG and NUP
(Cobb et al 2003)
Gingival and periodontal diseases

44. Gingival and periodontal diseases
NUP
Soft tissue necrosis,
Rapid periodontal
destruction
Bone is often
exposed, resulting in
necrosis
Sequestration
NUG

45. Riley et al 1992
85 - periodontally healthy
59 - gingivitis
54 - mild, moderate, or advanced periodontitis
none had NUG; and 2 - NUP
NUP in only 6.3% patients out of 700 HIV-positive
individuals (Glick et al 1994)
Patients with <200CD4 cells are 20.8 times more likely
to have NUP (Rams et al 1991)
Gingival and periodontal diseases

46. Treatment
• Meticulous oral hygiene procedures
• In severe cases, antimicrobial therapy (metronidazole
250mg, two tablets taken immediately followed by one
tablet QID for 5-7 days)
Gingival and periodontal diseases

47. Necrotizing ulcerative stomatitis
Extension into the adjacent bone osteonecrosis and
sequestration (similar to noma)
May occur separately or as an extension of NUP
Treatment
• Antibiotics (metronidazole)
• CHX mouthrinses
• If osseous necrosis has occurred then removal of
affected bone
Gingival and periodontal diseases

48. Chronic periodontitis
Maeley et al 2004, Barr et al 1992
Lamster et al 1994
Robinson et al 2000
Maticic et al 2000
Drinkard et al
Aichelmann-Reidy et al 2010
Treatment
Gingival and periodontal diseases

50. Periodontal treatment protocol
Health status
Health history, physical evaluation, and consultation with
physician
• What is the CD4+ T4 lymphocyte level?
• What is the current viral load?
• How do current CD4+ T4 cell and viral load counts differ from previous
evaluations?
• How often are such tests performed?
• How long ago was the HIV infection identified?
• Is it possible to identify the approximate date of original exposure?
• Is there a history of drug abuse, sexually transmitted diseases, multiple
infections, or other factors that might alter immune response?
• What medications is the patient taking? Does the patient describe or
present with possible adverse side effects from medications being
taken?

51. Infection control measures
Risk for acquiring as well as transmitting infections
Universal precautions
Sterilisation
Periodontal treatment protocol

52. Goals of Therapy
Restoration and maintenance of oral health, comfort, and
function
Conservative, nonsurgical periodontal therapy
Performance of elective surgical periodontal procedures
Thrombocytopenia
Periodontal treatment protocol

53. Maintenance Therapy
Prevent relapse after successful treatment of an acute
opportunistic infection
Recall visits
Blood and other medical laboratory tests
Periodontal treatment protocol

54. Psychologic factors
HIV infection of neuronal cells
Patients confidentiality
Periodontal treatment protocol

55. Conclusion
A chronic progressive process with a variable period of
clinical latency but no microbial latency. Knowledge of
the pathogenesis and the natural history of progression
is valuable in diagnosis as well as management

56. References
Mark Ryder. An update on HIV and periodontal disease. J
Periodontol 2002; 73: 1071-1078
Shilpa Kolhatkar, Syed Khalid, Anne Rolecki, Monish Bhola,
and James R. Winkler Immediate Dental Implant Placement in
HIV-Positive Patients Receiving Highly Active Antiretroviral
Therapy: A Report of Two Cases and a Review of the
Literature of Implants Placed in HIV-Positive Individuals. J
Periodontol 2011;82:505-511.
Patriciaa Murray Periodontal diseases in patients infected by
human immunodeficiency virus. Periodontology 2000 1994;
Vol. 6: 50-67

57. References
Michael T. Yin, Jay F. Dobkin & John T. Grbic. Epidemiology,
pathogenesis, and management of human immunodeficiency
virus infection in patients with periodontal disease.
Periodontology 2000 2007; Vol. 44: 55–81
Mary E. Aichelmann-Reidy, Dena L. Wrigley, and John C.
Gunsolley HIV Infection and Bone Loss Due to Periodontal
Disease. J Periodontol 2010;81:877-884.
Lauren L. Patton, Daniel A. Shugars, Arthur J. Bonito. A
systematic review of complication risks for HIV-positive
patients undergoing invasive dental procedures. J Am Dent
Assoc, Vol 133, No 2, 195-203

58. References
Walter Hall. 3rd edition. Decision making in Periodontology.
Mosby
Ananthnarayan R, Jayaram Paniker. 5th edition. Textbook of
microbiology. Orient Longman
Newman, Takei, Klokkevold, Carranza. 10th edition.
Carranza’s Clinical Periodontology. W. B. Saunders
Company.

59. ……Thank you